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The thyroid gland, located in the front of the neck, has two main functions—to secrete thyroid hormones and to secrete calcitonin.1 The thyroid gland operates via a negative feedback mechanism to synthesize thyroid hormones.2 The hypothalamus produces thyrotropin-releasing hormone (TRH) which then stimulates the pituitary to release thyroid-stimulating hormone (TSH). TSH, also known as thyrotropin, then stimulates the synthesis and release of thyroid hormones from the thyroid gland. Formation of thyroid hormones requires iodination of tyrosine residues by thyroid peroxidase to produce monoiodinated and diiodinated residues that couple to form triiodothyronine (T3) and levothyroxine (T4).3 Circulating levels of these hormones regulate the amount of TSH secreted. While the thyroid gland is responsible for the production of all T4, only 20% of T3 is secreted by the thyroid. Peripheral conversion of T4 to T3 forms the majority of T3. T3 is more potent, less bound to plasma proteins, and has a greater affinity for the thyroid receptor.2,3 Thyroid hormones affect multiple organ systems throughout the body (Table 59-1).1-4 Alterations in these hormone concentrations along with changes in TSH will lead to hyper- or hypothyroidism.2 (Table 59-2)

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TABLE 59-1 Effects of Thyroid Hormones
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TABLE 59-2 Overview of Thyroid Disorders
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Pathophysiology/Epidemiology

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Hyperthyroidism occurs when excessive thyroid hormones are produced.5 The majority of cases of hyperthyroidism (50%-80%) occur due to Graves disease, an autoimmune condition in which antibodies form against the thyrotropin receptor and stimulate the production of thyroid hormones.5,6 The remaining cases of hyperthyroidism occur due to a wide variety of reasons.2,5,6,7 (Table 59-3)

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TABLE 59-3 Causes of Hyperthyroidism and Hypothyroidism

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